Autoimmune disease after neonatal injection of semi-allogeneic spleen cells in mice: involvement of donor B and T cells and characterization of glomerular deposits.

Balb/c neonates injected with semi-allogeneic (A/J x Balb/c) F1 hybrid spleen cells develop an autoimmune disease associated with an immune-complex glomerulonephritis. The successful induction and maintenance of B cell chimerism is required for the occurrence of autoimmunity. The percentage of chimeric mice displaying autoimmune features increases in parallel with the number of cells injected at birth. T cell depleted inocula although readily inducing B cell chimerism were found unable to induce hypergammaglobulinaemia, circulating immune complexes and glomerulonephritis. IgG1 is the most and IgG3 the least represented IgG isotype among the immunoglobulins deposited in the glomeruli. Immunoglobulins bearing donor (A/J) allotype are detected in the glomeruli of six out of 11 chimeric mice. Rheumatoid factor activity is significantly concentrated within the immunoglobulins eluted from the kidneys, whereas anti-DNA activity is not.